CJC-1295: research overview

The short version

CJC-1295 is a laboratory-built copy of the first 29 amino acids of growth-hormone-releasing hormone — the signal the brain normally sends to the pituitary gland to make it release growth hormone. Four amino acids in that copy were swapped for sturdier ones, so that enzymes in the blood cannot take it apart as quickly.

The more consequential change is on the tail. In the long-acting version, a chemical handle latches permanently onto albumin, the most abundant protein in the bloodstream. The peptide then travels attached to a protein that circulates for weeks, and a single dose keeps growth hormone and IGF-1 elevated for days rather than minutes ^[9].

Two different molecules are sold under this one name. The version with the albumin handle is called DAC; the version without it, often labelled Modified GRF 1-29, is short-acting. They behave very differently, and confusing them makes every reported effect uninterpretable.

CJC-1295 is not approved anywhere. Its published human record is a handful of early pharmacology studies ^[8][9][10], and the original commercial development programme was discontinued.

What it is

CJC-1295 is a synthetic analog of human growth-hormone-releasing factor built on residues 1 to 29, hGRF(1-29), carrying four amino-acid substitutions: D-alanine at position 2, glutamine at 8, alanine at 15 and leucine at 27. Those four stabilise the alpha-helix and block cleavage by dipeptidylpeptidase-IV as well as deamidation and oxidation — the three routes by which the native peptide is normally destroyed.

In the DAC variant, short for Drug Affinity Complex, a C-terminal lysine is functionalised with a maleimidopropionyl linker. That linker undergoes a Michael addition with the free thiol on cysteine-34 of circulating serum albumin, forming a covalent peptide-albumin conjugate whose plasma half-life approaches that of albumin itself ^[12]. The no-DAC form keeps the four substitutions and omits the albumin handle; it is short-acting, and it circulates under the names Modified GRF 1-29 and Mod GRF 1-29.

The compound appears in the literature under a spread of aliases — CJC-1295 DAC, DAC:GRF, hGRF(1-29)-albumin bioconjugate, tetrasubstituted GRF(1-29) — which is part of why the DAC and no-DAC forms are so routinely conflated in commercial listings.

It has no approved human indication in any jurisdiction and is handled as a research chemical.

How it works

CJC-1295 binds the growth-hormone-releasing hormone receptor on anterior-pituitary somatotroph cells. Receptor occupancy activates Gs-coupled adenylyl cyclase signalling through cAMP and protein kinase A, which drives both synthesis and pulsatile release of growth hormone. Circulating growth hormone in turn raises hepatic production of insulin-like growth factor 1.

The interesting pharmacology is in the duration. Because the DAC conjugate persists for days, receptor stimulation is effectively continuous, and the obvious question is whether continuous stimulation flattens the natural rhythm of growth hormone secretion into a plateau. It does not. In healthy men given a single subcutaneous dose, the frequency and magnitude of pulsatile secretion were unaltered while basal and mean concentrations rose ^[10]. Pulsatility survives, which matters because the downstream effects of growth hormone are pattern-sensitive and not simply concentration-driven.

The design principle behind the albumin conjugate was demonstrated directly in rats: a series of hGRF(1-29) analogs bearing a maleimidopropionyl-lysine handle were screened, and the lead compound produced a four-fold increase in growth hormone area-under-curve over two hours compared with unconjugated hGRF(1-29), remained detectable in plasma beyond 72 hours, and showed enhanced in-vitro stability against dipeptidylpeptidase-IV ^[12].

What the research shows

Duration and magnitude in healthy adults. Single subcutaneous doses of 30 or 60 micrograms per kilogram in healthy adults aged 21 to 61 produced dose-dependent two- to ten-fold increases in mean plasma growth hormone lasting six days or more, and one-and-a-half- to three-fold increases in IGF-1 lasting nine to eleven days. After multiple doses, IGF-1 remained above baseline for up to 28 days. The estimated half-life of the compound was 5.8 to 8.1 days ^[9]. Those are the numbers that define the molecule.

Pulsatility preserved. In healthy men aged 20 to 40, a single subcutaneous dose of 60 or 90 micrograms per kilogram raised trough growth hormone approximately 7.5-fold, mean growth hormone by about 46% and IGF-1 by about 45% one week later, while the frequency and magnitude of pulsatile secretion were unchanged ^[10].

Measurable downstream signature. In 11 healthy young men, administration shifted the serum proteome — apolipoprotein A1 and a transthyretin isoform decreased, a C-terminal albumin fragment and immunoglobulin and beta-haemoglobin species increased — and the immunoglobulin and albumin-fragment signal correlated linearly with IGF-1 ^[8]. The study was designed to identify biomarkers of growth-hormone-axis activation, and it did.

Dose interval in a knockout model. In GHRH-knockout mice, 2 micrograms given once every 24 hours fully normalised body weight and length, while dosing every 48 to 72 hours was progressively less effective. Treatment raised pituitary growth hormone messenger RNA ^[11]. The finding establishes that a long-acting analog on a once-daily schedule is sufficient to restore growth-hormone-dependent growth in an animal that cannot make its own releasing hormone.

The albumin-conjugate proof of principle. Four-fold growth hormone area-under-curve over unconjugated peptide in rats, plasma detection beyond 72 hours, and demonstrated dipeptidylpeptidase-IV resistance in vitro ^[12].

Where it actually turns up. CJC-1295 was structurally identified by high-resolution tandem mass spectrometry as the active ingredient of an unknown preparation labelled only as GHRH, seized in an anti-doping context ^[7]. That is a fact about the supply chain rather than about the pharmacology, and it belongs on this page for exactly that reason.

Context. A 2025 review in Nature Reviews Endocrinology synthesises the pharmacology of growth-hormone-releasing hormone and its synthetic analogues as a class — receptor signalling, the design rationale for long-acting analogues, and their therapeutic and investigational landscapes ^[6]. It is the current framing document for everything on this page.

Reported effects, cautions and safety

The block that follows is anecdotal, not clinical evidence: what people using CJC-1295 outside any trial describe to one another. It was not measured, not controlled and not verified, the material was of unknown provenance, and no amounts appear here.

Better and deeper sleep is the most commonly reported effect and often the first one noticed, which at least rhymes with the biology, since growth hormone is released predominantly during deep sleep. Faster recovery from hard training and less lingering soreness form the next cluster. Gradual fat loss around the midsection, a leaner look, and better muscle retention while dieting are frequently described, always alongside diet and training that would confound any such observation. More daytime energy, sharper focus and firmer-feeling skin appear occasionally and inconsistently — some users report the opposite.

On the adverse side, holding extra water is the most commonly reported complaint, described as bloating or puffiness in the hands and face, and community accounts are consistent that it is more pronounced with the long-acting DAC form than with the short-acting one. Tingling or numbness in the fingers, likened to mild carpal tunnel and generally attributed to that same fluid retention, is the second. Injection-site reactions, flushing or a warm head-rush around the time of a dose, headache, fatigue or drowsiness, increased hunger — reported mainly when the compound is paired with a ghrelin-receptor agonist rather than used alone — and self-reported upward drift in blood sugar round out the list. None of it is trial data.

Cautions grounded in mechanism and literature. CJC-1295 has never been approved for human use by any major regulator, and the published human evidence stops at a small number of early pharmacology studies ^[9][10]. There are no large or long-term trials in healthy adults establishing either safety or efficacy, and the compound should be read as investigational rather than as a therapy with an unfavourable label.

Sustained elevation of growth hormone and IGF-1 carries the class concern. Population epidemiology links higher circulating IGF-1 to a modestly increased risk of certain cancers; that is an association drawn from population data, not evidence that this compound causes cancer. The relevance here is duration — the DAC form keeps IGF-1 elevated for days after a single dose and for weeks after repeated ones ^[9], so exposure is not comparable to a short pulse.

Growth hormone makes the kidneys retain sodium and water, which expands fluid volume and plausibly explains both the swelling and the nerve-compression symptoms people describe. Growth hormone is also glucose-sparing, so sustained axis stimulation can reduce insulin sensitivity; no controlled human glycaemic dataset exists for CJC-1295 itself.

In 2024 briefing materials for the Pharmacy Compounding Advisory Committee, the Food and Drug Administration cited immunogenicity — the risk that the body mounts an immune response to the peptide — among the safety concerns underlying its decision not to recommend CJC-1295 for the Section 503A compounding bulks list. The current class review reinforces that long-acting, albumin-binding designs raise such considerations ^[6]. This is a regulator-level concern rather than a settled clinical finding.

The original long-acting programme ran a Phase 2 trial in HIV-associated visceral obesity that was discontinued, and a patient death during the development era is frequently cited alongside the halted programme. The public record does not establish that CJC-1295 caused that death, and this desk does not assert that it did. What the record does establish is that the drug never advanced to approval.

Finally, the DAC and no-DAC forms are routinely sold and discussed as though they were interchangeable ^[12]. They are not: one acts for days, the other for minutes to hours, and the longer duration is what drives the more sustained fluid retention, glycaemic drift and IGF-1 exposure. Any reported effect is uninterpretable without knowing which form produced it.

Where it fits in the growth hormone axis

CJC-1295 is the lead compound on this desk because it is the clearest illustration of what the growth-hormone-axis literature is actually about. Every headline number attached to it is a hormone concentration or a duration: two- to ten-fold growth hormone, nine to eleven days of raised IGF-1, a half-life of 5.8 to 8.1 days ^[9]. Not one of them is a body-composition measurement in a healthy adult, because no such study was ever run.

Set against tesamorelin, which shares its receptor, the difference is developmental rather than pharmacological. Both are engineered GHRH analogues protected against dipeptidylpeptidase-IV. One was taken through a full programme to approval for a defined population and a defined endpoint ^[13][14]; the other was discontinued and now circulates as a research chemical. The molecules are cousins; their evidence bases are not comparable.

Set against ipamorelin, the difference is mechanistic: a releasing-hormone receptor rather than a ghrelin receptor, days rather than minutes, sustained elevation rather than a single 40-minute pulse ^[4]. The two are complementary at the level of receptor biology, which is the entire basis of the pairing people discuss — and there is still no trial of that pairing for any outcome whatsoever.